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Drugs: beta-blockers
- from Medical topics
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- By Sari D. Schwartz, Uniformed Services University of the Health Sciences, David S. Krantz, Uniformed Services University of the Health Sciences
- Edited by Susan Ayers, University of Sussex, Andrew Baum, University of Pittsburgh, Chris McManus, Stanton Newman, Kenneth Wallston, John Weinman, Robert West
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- Book:
- Cambridge Handbook of Psychology, Health and Medicine
- Published online:
- 18 December 2014
- Print publication:
- 23 August 2007, pp 683-685
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- Chapter
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Summary
Beta-blockers are a class of drugs that selectively compete for and inhibit binding at the beta-adrenergic subset of receptors of the sympathetic nervous system (Middlemiss et al., 1981; Patel & Turner, 1981). Beta-adrenergic receptors are primarily located in the heart and in the smooth muscle of the blood vessels and the lungs, but also exert metabolic and other effects. The beta-blockers are structurally similar to the body's adrenergic neurotransmitters, norepinephrine and epinephrine, and they exhibit their greatest effects during periods of intense sympathetic nervous system (SNS) activation. Therefore, the most common clinical use of these drugs is for the treatment of cardiovascular disorders, including hypertension and manifestations of ischaemic heart disease such as angina pectoris and cardiac arrhythmias (Frishman, 1980; Patel & Turner, 1981; Weiner, 1985).
However, since the introduction of these drugs and their wide therapeutic use, a variety of both desirable and unwanted psychological effects have been observed. One of the most frequently noted beneficial effects has been the reduction of reported anxiety by individuals in certain acutely stressful situations (e.g. performing before an audience or dental surgery) that are normally accompanied by several somatic manifestations of arousal (Frishman et al., 1981; Noyes, 1982; Elman et al., 1998). There have also been some reports that chronic beta-blocker therapy might lessen anger and irritability or ‘coronary-prone’ behaviour pattern (Schmeider et al., 1983; Krantz & Durel, 1983; Fedorets et al., 2004).
Hostility and Type A behaviour in coronary artery disease
- from Psychology, health and illness
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- By Willem J. Kop, University of Maryland Medical Center, David S. Krantz, Uniformed Services University of the Health Sciences
- Edited by Susan Ayers, University of Sussex, Andrew Baum, University of Pittsburgh, Chris McManus, Stanton Newman, Kenneth Wallston, John Weinman, Robert West
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- Book:
- Cambridge Handbook of Psychology, Health and Medicine
- Published online:
- 18 December 2014
- Print publication:
- 23 August 2007, pp 119-124
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- Chapter
- Export citation
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Summary
Historical perspective and early research
Systematic research on behavioural patterns related to increased risk of coronary artery disease (CAD) and its clinical manifestation as myocardial infarction was initiated by Friedman and Rosenman in the 1950s. The Type A Behaviour Pattern (TABP) was documented to be predictive of future myocardial infarction. TABP is defined as: ‘an action-emotion complex that can be observed in any person who is aggressively involved in a chronic, incessant struggle to achieve more and more in less and less time, and if required to do so, against the opposing efforts of other things or persons …’ (Friedman & Rosenman, 1959). Later research (reviewed below) has documented that hostility may be the ‘toxic’ component of TABP. Type A behaviour is characterized by an excessive competitive drive, impatience, hostility and vigorous speech characteristics. The complement of TABP was called Type B behaviour and was described as the relative absence of Type A characteristics.
The early reports by Friedman, Rosenman and co-workers have resulted in numerous epidemiological and experimental investigations on the relationship between TABP and manifestations of coronary artery disease. In the 1960s and 1970s, most epidemiological studies supported the association between TABP and risk of future coronary artery disease (CAD) in men and women. The magnitude of these associations was comparable to that of traditional risk factors for CAD and also independent of these factors, such as hypertension and elevated lipid levels.